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Benazepril, an angiotensin converting enzyme inhibitor: drug interaction with salbutamol and bronchial response to histamine in normal subjects
Author(s) -
Bauer K. G.,
Brunel P.,
Nell G.,
Quinn G.,
Kaik G. A.
Publication year - 1997
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.1997.t01-1-00633.x
Subject(s) - benazepril , salbutamol , placebo , medicine , propranolol , histamine , pharmacology , angiotensin converting enzyme , endocrinology , asthma , blood pressure , alternative medicine , pathology
Aims To investigate the effect of the angiotensin converting enzyme inhibitor, benazepril, on pulmonary function. Methods We investigated the influence of benazepril, on lung function and the interaction with inhaled salbutamol (0.1 to 6.6 mg) and histamine (0.03 to 30.69 g l −1 ) in normal subjects. Benazepril 20 mg, salbutamol 8 mg, propranolol 160 mg, and placebo were given orally once daily over 10 days. Results On day 8, there was no difference in the area under the salbutamol dose‐response curves between benazepril, placebo and oral salbutamol (P >0.05), propranolol shifted the curves to the right (P<0.05). On day 10, histamine challenge resulted in following PD 35 sGaw values (geometric mean and 95% CI): with placebo 1.02 (0.95–1.09) g l −1 , benazepril 1.04 (0.99–1.08), salbutamol 1.19 (1.13–1.25), propranolol 0.57 (0.50–0.65). Conclusions Benazepril had no influence on baseline lung function, caused no interaction with inhaled salbutamol and the bronchial response to histamine was similar to placebo. However, our findings in normal subjects cannot be extrapolated automatically to asthmatics.